1. Neuroscience
Download icon

Adult-born granule cells mature through two functionally distinct states

  1. János Brunner
  2. Máté Neubrandt
  3. Susan Van-Weert
  4. Tibor Andrási
  5. Felix B Kleine Borgmann
  6. Sebastian Jessberger
  7. János Szabadics  Is a corresponding author
  1. Institute of Experimental Medicine, Hungarian Academy of Sciences, Hungary
  2. University of Zurich, Switzerland
Short Report
  • Cited 28
  • Views 3,121
  • Annotations
Cite this article as: eLife 2014;3:e03104 doi: 10.7554/eLife.03104

Abstract

Adult-born granule cells (ABGCs) are involved in certain forms of hippocampus-dependent learning and memory. It has been proposed that young but functionally integrated ABGCs (4-weeks-old) specifically contribute to pattern separation functions of the dentate gyrus due to their heightened excitability, whereas old ABGCs (>8-weeks-old) lose these capabilities. Measuring multiple cellular and integrative characteristics of 3-10 weeks old individual ABGCs, we show that ABGCs consist of two functionally distinguishable populations showing highly distinct input integration properties (one group being highly sensitive to narrow input intensity ranges while the other group linearly reports input strength) that are largely independent of the cellular age and maturation stage, suggesting that 'classmate' cells (born during the same period) can contribute to the network with fundamentally different functions. Thus, ABGCs provide two temporally overlapping but functionally distinct neuronal cell populations, adding a novel level of complexity to our understanding of how life-long neurogenesis contributes to adult brain function.

Article and author information

Author details

  1. János Brunner

    Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary
    Competing interests
    The authors declare that no competing interests exist.
  2. Máté Neubrandt

    Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary
    Competing interests
    The authors declare that no competing interests exist.
  3. Susan Van-Weert

    Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary
    Competing interests
    The authors declare that no competing interests exist.
  4. Tibor Andrási

    Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary
    Competing interests
    The authors declare that no competing interests exist.
  5. Felix B Kleine Borgmann

    University of Zurich, Zurich, Switzerland
    Competing interests
    The authors declare that no competing interests exist.
  6. Sebastian Jessberger

    University of Zurich, Zurich, Switzerland
    Competing interests
    The authors declare that no competing interests exist.
  7. János Szabadics

    Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary
    For correspondence
    szabadics.janos@koki.mta.hu
    Competing interests
    The authors declare that no competing interests exist.

Ethics

Animal experimentation: All experimental procedures were performed in accordance with the ethical guidelines of the Institute of Experimental Medicine Protection of Research Subjects Committee (permission: 22.1/1760/003/2009) and were approved by the local virus safety committee.

Reviewing Editor

  1. Gary L Westbrook, Vollum Institute, United States

Publication history

  1. Received: April 16, 2014
  2. Accepted: July 23, 2014
  3. Accepted Manuscript published: July 24, 2014 (version 1)
  4. Version of Record published: August 13, 2014 (version 2)

Copyright

© 2014, Brunner et al.

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.

Metrics

  • 3,121
    Page views
  • 308
    Downloads
  • 28
    Citations

Article citation count generated by polling the highest count across the following sources: Scopus, Crossref, PubMed Central.

Download links

A two-part list of links to download the article, or parts of the article, in various formats.

Downloads (link to download the article as PDF)

Download citations (links to download the citations from this article in formats compatible with various reference manager tools)

Open citations (links to open the citations from this article in various online reference manager services)

  1. Further reading

Further reading

    1. Neuroscience
    Lorenz Deserno et al.
    Research Article Updated

    Dopamine is implicated in representing model-free (MF) reward prediction errors a as well as influencing model-based (MB) credit assignment and choice. Putative cooperative interactions between MB and MF systems include a guidance of MF credit assignment by MB inference. Here, we used a double-blind, placebo-controlled, within-subjects design to test an hypothesis that enhancing dopamine levels boosts the guidance of MF credit assignment by MB inference. In line with this, we found that levodopa enhanced guidance of MF credit assignment by MB inference, without impacting MF and MB influences directly. This drug effect correlated negatively with a dopamine-dependent change in purely MB credit assignment, possibly reflecting a trade-off between these two MB components of behavioural control. Our findings of a dopamine boost in MB inference guidance of MF learning highlight a novel DA influence on MB-MF cooperative interactions.

    1. Developmental Biology
    2. Neuroscience
    Qiuling Li et al.
    Research Article Updated

    Although many genes are known to influence sleep, when and how they impact sleep-regulatory circuits remain ill-defined. Here, we show that insomniac (inc), a conserved adaptor for the autism-associated Cul3 ubiquitin ligase, acts in a restricted period of neuronal development to impact sleep in adult Drosophila. The loss of inc causes structural and functional alterations within the mushroom body (MB), a center for sensory integration, associative learning, and sleep regulation. In inc mutants, MB neurons are produced in excess, develop anatomical defects that impede circuit assembly, and are unable to promote sleep when activated in adulthood. Our findings link neurogenesis and postmitotic development of sleep-regulatory neurons to their adult function and suggest that developmental perturbations of circuits that couple sensory inputs and sleep may underlie sleep dysfunction in neurodevelopmental disorders.